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Genetic Variants in NOS2 and CCL2 Modulate Risk of Post-COVID-19 Hyperglycemia via Immune-Metabolic Interactions
Ganyalak Chaimaha1, Nipaporn Teerawattanapong2,3, Kaweeraphat Chaithaisong4
1Graduate Program in Immunology, Department of Immunology, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand, mahidol.ac.th.
Genetic variations in innate immunity may increase the risk of hyperglycemia after COVID-19. Specific gene variants in NOS2 and CCL2 were linked to higher odds of developing hyperglycemia post-infection.
Area of Science:
- Immunogenetics
- Metabolic Disorders
- Infectious Disease Epidemiology
Background:
- Hyperglycemia is a common post-COVID-19 complication, but the underlying host factors are not fully understood.
- Investigating genetic predispositions can elucidate mechanisms behind heterogeneous metabolic outcomes after coronavirus disease 2019 (COVID-19).
Purpose of the Study:
- To examine the association between innate immune genetic polymorphisms and hyperglycemia in post-COVID-19 patients.
- To identify specific genetic variants contributing to metabolic dysregulation following COVID-19 infection.
Main Methods:
- A cohort study of 471 adults with prior mild-to-moderate COVID-19 was conducted.
- Participants were classified as normoglycemic or hyperglycemic based on HbA1c levels.
- Genotyping focused on innate immune-related genes, with statistical analysis using multivariable logistic regression.
Main Results:
- Hyperglycemic individuals were older, had higher BMI, more comorbidities, and elevated inflammatory markers.
- Significant associations with hyperglycemia were found for variants in NOS2 (rs4795067, rs35051118) and CCL2 (rs28730833).
- Specific NOS2 and CCL2 variants were linked to increased or decreased odds of developing hyperglycemia post-COVID-19.
Conclusions:
- Innate immune genetic variations may play a role in the development of hyperglycemia after COVID-19.
- Further independent validation is necessary to confirm the role of identified genetic polymorphisms in post-COVID-19 hyperglycemia.
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